Unleashing Breast Cancer Progression: miR-455-5p's Targeting of SOCS3 Drives Proliferation, Migration, and Invasion

Author:

Li Xin12,Peng Bing3,Li Jian4,Tian Mi5,He Lili1

Affiliation:

1. Department of Thyroid and Breast Surgery, Jingmen City People's Hospital, Jingchu University of Technology, Jingmen, Hubei, P.R. China

2. Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Universiti Malaysia Sabah, Jalan UMS, 88400Kota Kinabalu, Sabah, Malaysia

3. Department of Oncology, Jingmen City People's Hospital, Jingmen, Hubei, P.R. China

4. Department of General Surgery, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, P.R. China

5. Forensic Appraisal Center of Jingmen Public Security Jingmen, Hubei, P.R. China

Abstract

Objective: We aim to investigate the regulatory mechanisms of miR-455-5p/SOCS3 pathway that underlie the proliferation, migration, and invasion of triple-negative breast cancer (TNBC) cells. Methods: Reverse transcription-quantitative PCR (RT-qPCR) was used to detect miR-455-5p expression in breast cancer tissues and cell lines. CCK8 and Transwell assays were conducted to assess the effects of miR-455-5p on breast cancer line proliferation, migration, and invasion. SOCS3 expression level in breast cancer tissues and cell lines was determined by qPCR and western blotting. The targeting relationship between miR-455-5p and SOCS3 was determined by dual luciferase reporter gene assay in different breast cancer cell lines. Finally, the upstream and downstream regulatory association between miR-455-5p and SOCS3 was confirmed in breast cancer cells by CCK8, western blot, and Transwell assays. Results: MiR-455-5p expression was up-regulated in breast cancer tissues; miR-455-5p regulates TNBC proliferation, migration, and invasion of TNBC. SOCS3 was the direct target of miR-455-5p and was down-regulated in breast cancer. Interference with SOCS3 reversed the inhibitory effect of the miR-455-5p inhibitor on breast cancer cells' malignant potential. Conclusion: MiR-455-5p promotes breast cancer progression by targeting the SOCS3 pathway and may be a potential therapeutic target for breast cancer.

Funder

Science and Technology Foundation of Jingmen City, Hubei Province, China

Publisher

Bentham Science Publishers Ltd.

Subject

Biochemistry,General Medicine,Structural Biology

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